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Cardiovascular

II

oooooooaoooooaoocoaaooaooooaaaaooaooaotoaaaaoaocooaots0

Dr. Donald Sefcik

Donald J. Sefcik is the Associate Dean at the chicago college of osteopathic Medicine (ccoM), Midwestern university (MWU), in Downers Grove, IL. He is a tenured professor and board certified in both Emergency Medicine and Family Medicine. From June L997 through May 2000, Dr. Sefcik served as Medical Director for the Physician Assistant Program, College of Health Sciences (CHS), at MWIJ. Dr. Sefcik,s lectures are based upon his experiences as a clinician and preceptor, tenure as a medical school faculty rnembero and his student assessment research.

Dr. Sefcik has practiced with physician assistants since 1988 and been involved in the clinical training of physician assistants since 1990. Prior to joining Midwestern University's faculty, Dr. Sefcik was a faculty member in
the Pharmacology Deparfinent at Butler University and in the Nursing Depaitment at Marian College, both in Indianapolis, Indiana. Dr. Sefcik has a Bachelor of Science in Pharmacy (1981), a Master of Science in Pharmacology (1994), both from Butler university, illd an MBA (May 2004) from Purdue University.

CME Resources Certification & Recertification Exam Review

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CertiJication & Recertifi.cation Exam Review

CME Resources 2004
Cardiovascular Medicine - II Ischemic Heart Disease and Heart Failure Donald J. Sefcik, D.O., FACOEP

Learning Objectives
Upon completion of this portion of the review course, the participant should be able to:

2. Present an overview of aortic aneurysms and dissection. 3. Define ischemic heart disease (II{D) and coronary artery disease (CAD). 4. List several risk factors associated with CAD and IHD. 5. Compare and contrast stabie angina, unstable angina and Prinzmetal's angina. 6. Discuss diagnostic modalities utilized in the evaluation of IHD. 7. Describe the events culminating in a myocardial infarction (MI). 8. Discuss EKG manifestations of myocardial ischemia/infarction. 9. IdentiSr high-risk patients for acute MI.
10. Describe how a myocardial infarction is definitively diagnosed. 1. Discuss indications for acute coronary thrombolysis. 12. Describe therapeutic options for an acute MI. 13. Describe the rationale for IIID drug therapy.
1

1.

Differentiate corrmon causes of chest pain.

14. Identify potential complications of myocardial infarction. 15. Describe pericarditis: etiologies, manifestations & management. 16. Cornpare and contrast puhnonary edema and heart failure. 17. Differentiate left-sided and right-sided heart failure. 18. Conpare and contrast systolic and diastolic heart failure. 19. Prescribe appropriate heahnent for acute pulmonary edema. 20. Prescribe appropriate therapy for left ventricular dysfunction.

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Certification and Recertification Exam Review Cardiology - II

2004

Case

A 44 year-old male presents for a "checkup". He denies any health problems. He discloses to you that he drinks "regularly", smokes 1.5 packs of cigarettes a day and doesn't exercise ever. His BMI is 33, His blood pressure is 168/102 mrn Hg. His fundoscopic examination is unremarkable. You do note that his PMI (point of maximal impulse) is located in the fifth, left intercostal space, near the midclavicular line.

Case 1.1 Which one of the following therapeutic regimens is the optimal choice for this patient?

A. metoprolol B, hydrochlorothiazide Sg
C, D.

enalapril

diltiazem

&l

bO"fu Can - 5-U,l:

lr:c-

:-!cr.irA

e \ J,w$t

E. lifestylemodification

e -\Z t^ v'5

Case 1.2 Eventually, you add propranolol to this patient's therapeutic regimen. Which of the following side effects is most likely?
A. proteinuria
B.

bradycardia

c. depression
D. cephalgia
E.

.- V r .l

morbilliform rash

\,g.,* ovvs

su\

,)Ae-

c6'*^ y=ll"t'{u

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Certification and Recertification Exam Review Cardiology - II

2004

Case 2 A 48 year-old hypeftensive female transfers to your practice. She has currently discontinued all medications because she was concerned that her former clinician "prescribed too many medications", although she was happy with his bedside manner during the delivery of her five children. She has a history of depression and hypercholesterolem ia.

Case 2.1 Which one of the following is the best beta-blocker for this patient?
A. propranolol
B.

c.
D. E,

timolol

pindolol

[L.t.r"r

.., acebutolol 'f>

Se\ ec'N\ ,''ol '.,\ n eW.\ TSq rnVr t\' L *Y ^t'

[c',

\n*dy

'6t1

ma& ntdl*-\

Case 2.2 Two weeks after the initiation of therapy for her hypertension, she returns complaining that when she coughs "she wets her pants". Which of the following medications was most likely started two weeks ago? A. reserprne
B.

clonidine

c. hydrochlorothiazide D. terazosin
E. diltiazem

d l\uoKpn

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Certification and Recertification Exam Review Cardiology - II

2004

Case 3 A 68 year-old hypertensive female presents complaining that her new antihypertensive medicaiion causes her to experience "skipping heart beats", swelling of her legs and headaches. Her blood pressure is 178/96 mm Hg, She has a grade lllA/l diastolic murmur,

u.,,)eneJ tr it pff,r*urt
Case 3.1 Which one of the following is the most likely cause for her murmur?

A.

aortic stenosis

B. aortic regurgitation C. mitral stenosis D. tricuspid stenosis E. pulmonic regurgitation

Case 3.2 Assuming that this patient was prescribed a calcium channel blocker, which of the following is LEAST likely the agent she was taking?

A.

;: i;ffiil; \ C. amlodipine
-

nifedioine

D. isradipine E. verapamil n$,r

,/

r:u\o.\
'

rr,+l"c),\^d^rt

.f,!.y,.r1r.'.J.'p. le'l: putt-{ t'aJorl",l^7}'r,

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Certification and Recertification Exam Review Cardiology - II

2004

Case 4

A 51 year-old male presents to your office after being discharged for a heart attack. He is currently taking one aspirin a day. You review his charts and note that he has a history of hypertension, gout and diabetes type 2. His echocardiogram in the hospital, prior to discharge, revealed an ejection fraction of 52%.

Case 4.1 Which one of the following antihypertensive agents is the best choice for this patient?

A. B.

hydrochlorothiazide

C. prazosin D. diltiazem E. propranolol

lisinopril

Ou-:\

nn

T.

Case 4.2 Which one of the following agents would most likely worsen his gout?

A. hydrochlorothiazide '-T\n;r.,,:flC C^ur<: h 1p"*t-,"-" B. clonidine C. methyldopa D. verapamil E. propranolol t)*,clu;'*- AgA =

\o^
T

o"J'
tI

t! ' Jta+ tt

d- t..-

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Certification and Recertilication Exam Review Cardiology _ II

2004

Gase 5

A 54 year-old male presents with a sudden loss of vision that began 30 minutes prior to arrival' He denies any trauma prior toirre visual ror.. i" oenies pain. Examination of his visual acuity reveals that,he r'trr iigl'rt perception oniy. L*"rination of the ipsilateral ?il::::::,:"":"3["j::]fifl?y 991eit a1o ,ignifi.rni ,ia,rowins of the retinar arreriores rhere are no cotton-woor

ipots oin"mo"rr.s;.

;p;,;;i;i;:"'r;.:'j:,:'??ffi:i,B

o,

crorni.r,,

Case 5,1 which one of the following, fundoscopic findings would be most supportive of the diagnosis that you suspeCt?
A. macular B. tortuous and dilated retinal veins c. retinal at"rilf" r"-grentation of blood D. an,increased cup:disc ratio (greaterihan E. isolated hyperemia of the naial naft of tne fundus

edema

4,,.-la
-:
-

lBoxcc.m.\) J 0.6)

kf^u*6 ot t;llLen * c crl'*- .---r:o\ L

Wt*l*:z'yd

AcJ. Ar-t'r^\ c'.-'(4'cttt = O, $n e-Ch trrnY f.,cl-* ''F

Case 5.2

which one of the following diagnostic study combinations would most likely reveal the etiology for this patient,s ophthZtmic
piobtem?

A.
D' E.

? c'

complete blood count and INR echocardiogram and carotid doppler studies cr scan of the brain and intraocrt.r pr"rrrre measurements fluoroscein staining and intraocur.i pr"rrrre measure,";;i; MRI scan of the briin and ,ortogrm

"n

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Certification and Recertilication Exam Review Cardiology - II

2004

Case 6 A 62 year-old male presents complaining of shortness of breath on exerlion for the past several weeks. He states that his "heart races in his chest" because he gets so short of breath. His chest x-ray is unremarkable. ljs-Hemoccult is negative. r unremarkable. His hemoglobin is 9.4 Gm/dL; McV is Tp fL; RDW is(0.8)

\!",,, r.x.r$n,. *" ,. cldr"''r'*r'''s {L^l "trln r ci. ,-., .,. {}^tt""t$' ,"N ,{ RDiq-' l-Case 6.1 Which one of the following is the most appropriate at this time? Tn^*,[dfr,
A. order a serum ferritin level, TIBC and reticulocyte count B. order a hemoglobin electrophoresis C. order both serum 812 and folate levels D. prescribe vitamin 812 E. prescribe a multivitamin supplement with vitamins A, B, C, E, and iron

,."l.u#

trlr.=1

ne\z T
\Case 7

c.

N,*-k i^r^"(it

Ac,"k

.Soo,\

loii *f

Ten days after an acute myocardial infarction, a 56 year-old female presents complaining of chest pain. The pain is worsened with inspiration. She denies shortness of breath. Physical examination revels a low-grade fever, bilaterally clear lungs, and a normal sinus rhythm without gallops, murmurs or rubs. An EKG reveals inferior q-waves, without evidence of ST segment displacement.

Drc*-$nr> -s/nulfo? =
Case 7.1 Which one of the following therapies is the most likely to be effective?

A. cephalexin 500 mg orally four times a day B. doxycycline 100 mg orally twice a day C. nitroglycerin sublingually @ibuprofen 600 mg orally four times a day E. warfarin Smg orally every morning

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Chest Pain
Principles:

4.

1. Any chest or abdominal pain complaint may be a manifestation of heart disease. 2. Accurate diagnosis is based upon interpretation of the patient's pain perception. 3. The diagnosis, often based solely on history, can be biased and/or misperceived.
Physicalfindings/ancillary tests may not be helpful, and may be misleading.

Non-Emerqent Etioloqies
Klinkman MS, Stevens D, Gorenflo DW. Episodes of care for Chest Pain J Fam Pract 1994;38:345

A. Musculoskeletal

36

o/o

Muscular Active patients "Sharp" pain Exacerbated with movement Tenderness(reproduciblesymptoms)

Skeletal (Costochondritis Tietze's syndrome) Commonly young women (African-American more commonly) Pain exacerbated with deep inspiration No history of repetitious activity/trauma lf NSAIDs taken - usually have reduced the symptoms Tenderness - more commonly left % costosternal margins eain is reproducible in 5 - 10 % of patients with acute cardiac ischemia

J<

B. Gastrointestinal

19 %

"-itis"

lk

Relationship to food Relief with antacids or eating G/ eocktailreso/yes pain in 5 - 10 % of patients with acute cardiac ischemia

Esophageal spasm "Squeezing" retrosternal Associated with

pain/discomfort \ ! - sr'-rt,,o1.. n-ro{.k_ {V 'icu GERD - * Esophogram fcJroxr.,rf l;wt Nutcracker of Corkscrew esophagus gsopdi\{],SuS

C. Cardiac - 16 o/o Typical angina (next section) MitralValve Prolapse "Sharp" or "Dull" pain Palpitations Mid-systolic click and murmur

r .

' -

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D.Psychosocial Anxiety

-9%

E. Pulmonary - 5o/o Bronchitis Pleurisy/Pleurodynia

. . .

F. Atypical

- 15

o/o

No etiology is clear

Ischemic Heart Disease

1.

fr*5* f:w'n*y ' S i'rrn';rr!z'Syndromes \J""aG- chest discomfort secondary to myocardiat isJfiemia .. T Stable Demand) Anqina V,3Crt,:u\ pr:'1"1"1 = t'''S\
Coronary
J+

-1*, *+^^t
.{r
q

Occurs with a fixed threshold of increased workload. Manifests as retrosternal chest discomfori, which may include radiation to the arm, back, neck or jaw, nausea, diaphoresis, shortness of breath, etc., precifitated by:

Exertion (generally) or Emotion (anger) or Eating........

Relieved with Rest (reducing workload) [usually discomfort lasts 5 - 15 minutes] or Nitroglycerin (NTG).

crricl '. -s a\wr"yS \ ;1'-1E"ir"5te- J Angina of new onset, angina at rest (or with less exertion), or a pattern of
l.Jnstabte (Supplv) Anqina fpreinfarction

anqinal C ,.>f n ei,o

,1g" increasing frequency, severity and duration of anginal episodes, requiring

. -.rG{ \ \t\" L ! t'.*1"* \periods of rest or more NTG to obtain relief of symptoms. Variant (Prinzmetal's) Anqina

longer

L ffr qt5 ,
-

rf\tJ6tv',ruu

-r g(5 ,g-'Y' ''* '

, ,io.sl.no& (*/'- oo"y,1,L fl."Anqina'Equivalent" . nt'J' *'9

-

.,c,k .a

ffSil:fil5ill?1 - .

L"-'S?:fiy';ffi:,?"JIii["iTI,:J:'T;:
,-+

ls.i6 rnfirs'\ r{ -p.tt-i"n:'

Cl"srr

Ofter6ySplgil dizziness, fatigue, or syncope 'rs

,y1 *r

*S,"niuJ*EA

g\.

] +U

,\c '-lrraA

due to transient myocardial ischemia.

pr'i.ll

Asymptomatic periods of myocardial ischemia. Silent Ml - more common in diabetics and the elderly.

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bl Myocardial lnfarq-tion

h Myocardial Cellular Death

Generally secondary to coronary artery thrombosis, resembling "angina" but typically greater in severity and duration, often not relieved with rest or nitroglycerin.

nequirements for diagnosis (2 of 3):

- A classic history - Evolutionary changes on EKG - Elevation of Cardiac Enzymes/Markers

* Year 2000 ACC/AHA Guidelines: ACS UA, NSTEMI and STEMI =

Clinical Presentation

Myo c ardi al i schem i a causes.'

A. the "classic discomfort" B, autonomic nervous system activation

SNS - diaphoresis; vasoconstriction [cool, clammy skin] PSNS - nausea; weakness [vagal effects]

C.

myocardial dysfunction: ventricular gallops (chamber compliance changes) dyskinesis (reduced cardiac output) rales (pulmonary edema) arrhythmias

Sa

gallop (atrial gallop)

A.

P ote nti al com pl i catio n

in cl ude :

B.
C. D.

arrhythmias [electrical - altered transmembrane ion flux] hypotension [mechanical - myocardial cellular dysfunction] embolism [mechanical - ventricular cavity thrombus formation]
pericarditis Iinflammatory] pulmonary edema/CHF [mechanical - myocardial cell dysfunction; valvular dysfunction; tamponade]

E.

The differential diagnosrs of acute chest pain resembling AMI includes:

A.

(,

\. -\-----

inflammation of pericardial sac pain; changes with position [reduced leaning forward]; odynophagia ,r-pleuritic pericardialfriction rub (may be intermittent) diffuse ST segment elevation
Pericarditis

----==--+

P\eotJr= T

Pc^l^kr$l f&{{L'.I r ' flc\cJ c la^nb

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I:**,i"J J,bry5- dcu,*,^ ,^;i* fiPe

B.

o pleuritic pain; pleural friction rub . SEiItGet with dyspnea triad - venostasis; hypercoagru*ilry' intimal injVry) @irchow's >-ffiAfrgradient I Al*rrl * n-:."r*l rrCo\ =T g*JF,n t .-. CXR - most commonly is normal . V/Q scan; Pulmonary angiogram - gold standard G\rut* :67rcrr .{ tt .

Pulmonary embolism

- pulmonary vascular

occlusive event

C.

. Secondary
COPD; Asthma;

Pneumothorax - gas in pleural space Primary (Spontaneous) - No underlying lung disorder Young males (tall and thin); Smokers; Valsalva Maneuvers

frs| b,ant
\
p{

{s*J

Pneumonia.,..

(* r"t t$bt nr"\ds ) tJ \/ '

o . r . . . r .

Simple lntrapleural space pressure is equal to atmospheric pressure Expiratory fitm rncreases visualization (loss of peripheral lung markings...) Tension Pleural defect acts as "one Way Valve" - prodUces positive pressure resulting in contralateral shifting of mediastinum; JVD; hypotension...... *** po not wait to get a chest x-ray Needle thoracostomy, zno ICS/MCL

!-

D. Pneumonia

pleuritic pain cough, sputum Produciion, fever chest x-ray and/or physical signs of consolidation

- lung consolidation

Aus"\}-- ?SaF\'\o^Y

E. Thoracic Aorlic dissection

. .
F.

begin as intimal tear - cleavage plane is within media commonly 50 - 70 year old males abrupt on - "tearing" or "ripping" - typicall(between the shoulder Classic physical features Unequal (absent) Pulses Focal neurologic deficits Signs of cardiac tamPonade **-geck's triad * fiugular venous distention, muffled heaft sounds, hypotension) Gold Standard - Aotlogram CXR (upright PA) - widened mediastinum - suggestive

Others

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1.

Definition

Myocardial cellular necrosis secondary to coronary artery occlusion, most commonly tlie result of thrombus formation upon an atherosclerotic plaque. Of acute chest pain
Entergency Department - 30 % patients = coronary ischemic event Primary Care ffice - 5 % patients coronary ischemic event

2. Pathophysiology a. HowAVhy does

it happen

i.

Etiology

Coronary artery thrombosis (most common) Ernbolic \ lrs c\ Coronary aneritis \-ra,io.w"K, '!ea'!f

event

Cocaine use

ii. Sx/Sx

Anginal type discomfort that is sustained/changed

Dyspnea common in elderly Associated nausea, vomiting, diaplioresis * Often confirsed with indigestion May auscultate an 54 gallop May demonshate signs of acute heart failure

b. Who's at

risk

(
Before age70 - Male > Female After age 70 - Male = Female

L*/

hr

i.
ii.

Maleffemale

'1V'.,

,"..'

Pz:opY I LltJ Y I O

;;

Age

Increased incidence with age (more common > 40 years old)

iii. Risk Factors - Family history premature coronary artery disease (CAD)
Hypertension Hypercholesterolemia
Cigarette smoking Diabetes mellitus

nnecl- ,,.r-,Jan5

Aging/Male sex (< 70 years old)

3. Differential Diagnosis 4. LaboratoryIK-Ray see prevlous

ott;,," t^*L.*l

EKG

- 50 %o are normaVnondiagnostic
May d

fi\'n

at

AMI presentation

firt J stung

3xJ

ST Elevation - Transmural

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DIFFEEENTIAL DIAGNOSIS OF *EKG CHANGES'

1.

T-Wave

Inversion:

Myocardial IschemiaAnfarction
Severe LVH or RVH with "Strain" Cardiomyopathies

Pericarditis Ilemorrhagic Stroke

i-

2.

ST Segment Elevation:

Acute Myocardial Ischemia/Infarction Pericarditis Ventricular Aneurysm

3.

QRS Changes @evelopment of Q

Wave):

Myocardial Infarction Septal Depolarization

Cardiomyopathies

)k'

,)b

t \f .t

WBC - Often demonstrates leukocytosis Chernistries - Associated risk factors Echocardiogram May demonstrate wall motion abnormalities (hypokinesis) CXR - identifies (rules out) other pathology Cardiac En4ymes fMarkers] - May Demonstrate cellular necrosis (CK, AST, LDH; Troponin; Myoglobin)

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Myocardial ischemia results when cellular oxygen demand exceeds oxygen supply. Myocardial oxygen demand is determined by (a) gontractility [inotropic state - a measure otttre toice of contraction], (b) heart rate fdetermines ATP utilization and oxygen consumption], and (c) ventricular wall striss [a product of ventricular wall thickness and intraventricular presiure].- Myocardial oxygen supply is dependent upon oxygen,calline capacity of the blood [determined by oxygenatioo anO fremoglobin contentl and coronary blood flow [a result of vascular tone, Iumen pui"ncy *a perfusion pressures].
Myocardial hypoxia causes increased anaerobic metabolism (an innacellular acidosis develops) and an impairment of the ATPase ion pumps (resulting in altered membrane ion movement - the EKG records these changes as T wave ilversion, ST segment displacement, and,/or anhythmias; if cell death occurs, Q waves may eventually develop). Ischemia of the entire thickness of the ventricular wall is termed transmural; ischemia of the innermost layer(s) of the ventricular wall is termed subendocardial ischemia. Historically, e wave infarctions were believed to represent myocardiai necrosis of a transmural nature, while Non-e-wave infarctions were believed to be the result of subendocardial myocardial infarctions. lnterestingiy, ST segment elevation represents transmural ischemia (an injury pattern) and will probably result ini Q-wave infarction, while ST segment depression represents subendocardial ischemia and may result in u lion-q-wave infarction. The development of abnormal Q waves (over a 2 - 24 hour period after the onset of clinical symptoms) is indicative of myocardial cellular necrosis.

Finaliy, although the initial mortality is lower in patients suffering Non-Q-wave infarctions than patients having Q-wave infarctions, during the subsequent months, the reinfarction rate and risk of death is greater in the patients suffering the Non-Q-wave infarctions.
Tvpical EI(G Evolution Pattern of Mvocartlial htfsrction

Acutely
Q-wave

< 24

hrs

24 - 48 hrs

Days later

Weeks later ST & T normalization Q wave persists

MI

sr elevation sr elevation

R waves reduced Q wave Q waves appear

T wave inversion ST normalization deepens Twave inverted

Non-Q-wave

MI

T wave inversion
ST depression

T waves normalize No Q waves

Abnormal ST Sesment Changes

The most definitive changes accompanying acute myocardial ischemia are ST segment alterations. Polarity changes ofthe T waves are less reliable. ST segment Elevation: Elevated if the ST segment is =/> I mm above the baseline, measured at 0.08 seconds (2 mm) after the J point Note:
the shape of the ST segment may be a clue:

.-* A f";-rol\ (tt) \-,, i -1 /^t* ll

{

a. b.

upward concavity ("smiiing") - benign ??? coved (downward concavity) - acute iniury ???

;L*
--ll**,fvt*-

f+ronc-,,..1r *,,^^--J:-r :-^L^-:^ r:-r--^.:^-l Causes: [transmural] myocardial ischemia [infarction] "*,".".

Prinzmetat'sangina

acute pericardiris ventricular aneurysm twperkalemia eariy repolarization ventricular hypertrophy myocarditis Bundle-branch blocks

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ST segment

Depression:

Depressed if the ST segmett is =l> I mm below the baseline, measured at 0.08 seconds (2 mm) after the J point

Note:

the slope of the ST segment depression may be:

a. b, c.

downsloping - most indicative (specific) horizontal - intermediate specificity upsloping - least definitive

Causes: [subendocardial] myocardial ischemia

Non-ST segment elevation AMI LVH "strain" pattern

digitaiis effects
Bundle-branch block hypokalemia; hypomagnesemia

***

Nonspecific ST-T wave changes

Alterations in the ST-T wave morphology that are not isoelectric and not normal, yet not abnormal enough to be labeled as ST segment elevation/depression and/or T wave inversion. Causes include: Myocardial Ischemia, ventricular enlargement, drug efflects, electrolyte disorders, acidosis, hypothermi4 hyperthermi4 hyperventilati on, medical illness

EKG Correlates of Myocardial Ischemia and Infarction

Emergency Medicine Reports

April 23, 2001

A. Focal changes (Inferior, Anterior, Lateral) reflect ischemic area(s). B. Elevation and depression demonstrate 'current of injury' pattern.

AMI location [LVl

Anterior wall
Anteriolateral Lateral

EKG leads

ST sesment chanpe elevation elevation elevation elevation

denression

vl -v4
V1

- V6 (+/- I and aVL)

I, aVL (+l- V5 and V6)

Inferior
Posterior

II.Itr

and aVF

Vl _V3

S
ED Interpretation
Normal Nonspecific Abnormal (nreviously documented) Abnormal (not oreviouslv documented Infarction

e\e./Sft/,-' Joe* nu\ nne,a^

n^f

AU<^At\

ED EKG Diasnosis and Diagnosis upon tr'inal Hospital Discharge Emergency Medicine Reports - April 23,2001

AMI
lo/o
3o/o

Unstable Ansina
4o/o

Noncoronarv Diasnosis
95%
7 5o/o

23o/o

7%
25o/o

48Vo
43o/o

45%
32Vo
14o/o

73%

t3%

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CARDIAC MARKERS
(Variable values in Literature)

TEST

TIME

DETECTION

TIME PEAK
12

24 hours

Myogrobin

(i.*,.'
--Tlt

caA

riwory

"rfff"rf

O*^tt'

8 hours

Smsll Heme proteht

Not speciJic

r-+ Troponin

nL-

t^ir)r"-\

Contrsctile Protein

{x* ^ t'on'\c 3-12hours

WA4:y>
5. Treatment Plan
a. Lifestyle changes

SpectJic Myocardial

cells

,3,.,ki',* :f t'

l0 -2|trours 1f 10 days,1 I rnu:r\ c('-<""l irc Jif-lrc f, (

Stop smoking Exercise program (as indicated) Modify coexistent risk factors (Chol, Blood sugar...) Control hypertension

Minimize stress
b. Nondlug Therapy

Diet - Low Cholesterol./Fat, Low Sodium Exercise program, as indicated

c. Treatment -

Acutely
1. Patient Position

a. Sitting

lncreases tidal volume Reduces work of breathing

Helps in pulmonary edema/CFIF 2. Oxygeriation

a. Patients should receive oxygen (maintain saturation

at=/> 95Yo)

b. Nasal prongs at 2-4 liters usually adequate. c. When oxygen saturation cannot be maintained:/> 950/o, obtain ABG,

or when other clinical diagnosis/therapy requires an ABG. Avoid ABG when possible, if patient is thrombolytic candidate.
3.

fV Access
a.

Two large-bore (16-18 gauge) sites recommended.

10

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lnCruA\+.ll, )
4. Monitors
a. Cardiac

b. Pulse oximetry c. Blood Pressure

5. Chest Pain
a.

Relief

\ .l l^+.^r\ S- .U prrlo^J , u-"rn yor't'/^'\ 6. Mortality Reduction a. Aspirin(unlesscontraindicated)

b.

Nitroglycerrn ^fta=o
Morphi'e

Oi J t'^'n'A'

* Ticlopidine (TICLID) * Clopidogrel (PLAVIX)

b.

Heparin * Unfractionated

* Low Molecular Weight Heparin (LMWII) o Less risk of bleeding r No dosage changes based on coagulation parameters IIb/IIIa Inhibitors

d,

Thrornboiytic agents (Choice ??) - Given < 70 minutes post-onset - mortality - L2 % - Given > 70 minutes post-onset- mortality - 9 % Indications

Typical Chest pain

sr t"ry;3'r"Hl'J",ftre,rimb);
> 2 mm (precordial) Symptoms < 6 - 12 hours (?? beyond in "stuttering" pattern) LBBB (new onse0

r r . o o r o . r r r r

.""E

Exclusionary Criteria Hemorrhagic CVA within past 6 months Recent head trauma or known intracranial mass Uncontrolled hypertension (> 180-2001> 110-120)

Major surgery within past 2 weeks Active or recent Gastrointestinal bleeding Bleeding disorder or anticoagulation Aortic dissection or pericarditis Noncompressable vessel puncture
Prolonged CPR Previous Streptokinase use (time dependent)

l1

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e. Beta- Blockade

later

initiated early - may limit or reduce size - minimizes reinfarct/arhythmias

f. ACE Inhibitors

Effect on LV remodeling and recurrent ischemia Post-AMI for reduced EF; clinical CF{F; wall motion abnormalities

Monitor for electrical/rnechanical cornplications

*

Electrical Any dysnhythmias

* Meehanissl

Pulmonary edema/Heart Failure Cardiogenic shock Pericarditis Dressler's syndrome Myocardial wall/Septal rupture LV Wall Aneurysm formation Thrombotic or embolic events
d. Surgery

Percutaneous transluminal angioplasty (PCTA)

Coronary angiography Coronary Artery Bypass Grafting (CABG)

6. Follow Up - Educating the patient about expectations

a.

Patient Education Must treat coexistent conditions Stop smoking Compliance with exercise, diet, medications, etc
Future Appointments

b.

Dictated by post-AMI course and complexity of coexistent conditions

c.

Emergency Visits Recurrence of chest discomfort Pain not relieved by Nitroglycerin Any decompensation/signs of complications

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PERICARDITIS
1. Definition

- Inflarnmatory changes of the pericardial sac surrounding

the heart

2. Pathophysiology
a.

HowAilhy does it happen

Etiology

i.

Idiopathic Viruses - Coxsackie, Echovirus, Adenovirus Bacteria - Haemophilus (esp. children) Fungal Uremia Neoplastic Autoimmune (SLE, Rheumatoid Arthritis.....) Dru g-induced (procainamide, hydralazine. . . ..) Post-AMI (Dressler's Syndrome) Acute Pericarditis
Chest pain

ii. Sx/Sx

usually sharp and pleuritic often reduced with sitting up/leaning forward may have associated pericardial friction rub Dyspnea, rales, tachypnea Fever, often with myalgias Odynophagia Cardiac dysrthl'rnias (often supraventricular tachycardias)

Pericardial Tamponade (more pronounced symptoms with acute/larger effusions)

Dyspnea, sometimes with cyanosis Distended neck veins Hypotension - often with thready pulsus paradoxus .L, s;s*r,t;<-

pulses -l by ) lc ,n.n rf\glS cn Quiet pericardium with diminished PMI ,nsp3$d,rr

dullness & bronchial breathing rnedial to tip of left scapula

Ewart's sign

b. Who's at

risk

i. MalelFemale ii. Age iii. Risk factors

Male > Female Adolescents & younger adults Dependent upon etiology (see above)

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3. Differential Diagnosis

Acute

MI

Pneumonia

Pleurisy Pulmonary Embolism

Pneumothorax

Aortic dissection
PancreatitisiCho lecystitis 4. LaboratoryD(-Ray

WBC - Leukocytosis
ESR Elevated (better to follow treatment and response) Cardiac En4,mes - may be elevated (epicarditis) CXR - may demonstrate pleural effusions/other diagnosis x large pericardial effusion - "waterbottle heart"

EKG
ntay show dffise/global ST segment elevation may show PR segment depression

Echocardiograrn - identifu pericardial effusion

5. Treatment Plan
a.

Lifestyle changes -

Activify limited by symptoms

b. Nondrug Therapy c. Rx

Aspjrin (in simple uncomplicated cases) May use otherNSAIDs

Some may require corLicosteroids (r/o Tuberculsosis. . ...)

d. Surgery

May require pericardiocentesis May require pericardiectomy

6. Follow Up

a. Patient Education
Up to i5% may expect recuffences Advise on signs of complications (pericardial effi.rsion) Compliance with Rx regimen

b.

Future Appointments

Follow-up in @2 weeks, unless worsens Follow-up CXR & EKG

c.

Emergency Visits S igrrs/Symptoms of decompensation

Respiratory/Cardiovascular dysfunction + Progressive/Acute dyspnea * Worsening chest pain * Dizzinessllightheadedness (signs of hypotension)

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Left Heart Failure

Dyspnea

Orthopnea PND
Rales Wheezes Frothy Sputum

lvarvn L_--.-__

[oRirc

*l
i i

53, (?S4), Tachycardia (?)

Fatigue 'Wealness

Manifestations of Hypoxemia (Tachy...)

Rieht Heart Failure

LT]NGS

Hepatic Congestion

IVD
Hepatojugular Reflux RUQ Pain
B

loating/As cites/Anorexia

Lower Extremity Edema

Fatigue
Weakness

Manifestations of Hypoxemia (Tachy...)

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HEART FAILIIRE
1.

Definition
Heart Failure is a nonspecific term.
Inability of the heart to pump adequate biood to meet the metabolic needs of the body. May be the result of "heart disease" (unable to pump) or the result of "excessive demands".
May be acute or chronic. May be systolic and/or diastolic in etiology.

2. Pathophysiology

HowMhy does it happen

Etiology Normal ejection fraction @2/3 ventricular volume. Myocardial dysfunction (Heart Failure) reduces ejection fraction. When the result is increased diastolic filling pressures, the organs that "empty" in the respective ventricular system become congested.
* Congestive Heart Failure (CHF)
a.

Primaty Hemt Disorders - usually result in contractile abnonnality - Coronary Heart Disease - Valvular Heart Disease - Cardiomyopathies

b. Excessiye Demands

- Increased pressure (afterload) - Increased volume (preload) - Increased tissue oxygen requirements (perfusion)

Heart Failure Glassification

ACC/AHA
A

Staqe
High Risk -for LVD
I

Patient Variables
HTN; CAD; DM Familv Historv Previous Ml; LVD Valvular Heart Disease Dyspnea and Fatigue Reduced exercise tolerance Marked symptoms at rest Maximaltherapv

NYHA

eft

ve

ntricu I ar dysfu n ction

Asymptomatic LVD

c
D

Symptomatic LVD

llIV

ilt

Refractory end-stage HF

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Svstol ic Versus Diastolic Dvsfunction

t;*c\rr-' Drotk'rP r-+ Fr$'i\t \

D;rr'$'Jd*

Systolic (Ejection disorder) [Ejection Fraction < 40%7

Etiology CAD

Diastolic (Filling disorder) fl mpaired ventricular relaxation

ra",d,VtkHTN crsr cc^-'pl. -tnii,\ & 'r s-1 Sli LVH [LVE] Valvular heart Disease h{-tt Chronic
"AS, AR, MR

lschemic lnjury (Ml)

EIOH history

Pathology

Reduced Ejection Fraction (EF) Dilated Ventricle Looks large on chest x-ray

Often Normal/Supranormal EF Altered ventricular filling Restrictive Ventricle Stiff and noncompliant ,,----."

, ,^!.Y!.{.-^F..^,*l^J
Clinical Changes
Reduced LV Elevated Pulmonary edema

EF * \r":oPCWP ,L.ru.r.{K
u

Reduced LV Prbssures "n DD.r Elevated Atrial Pressures :'l\as Pulmonary Edema DyspneaMeakness/Fatigue Rales/Peripheral Edema Sa gallop

\j

Symptomatology
Signs

Dyspn ea/Weakness/Fatig

Rales

Ssgallop
Reduced pulse pressure

Acute Tx

Vasodilators Loop Diuretics lnotropic agenis Reduced Na intake ACEIA/asodilators Diuretics (prn) Di goxin/Beta-B lockers

Vasodilators Judicious Diuretic Use lnotropic agents Reduced Na intake

ACEI

Chronic Tx

Diuretics (prn) Beta-Blockers/CCB

o ?ffe--t6;k
?rfu: c'.\\&>

*ne

*rLo:L,
?

Vroo.e v'r\bar\g

c" tc-nt e-",,*,ogr6arr1 (' '( CKu c,^-#''*r en\cgr"--t'r\ {"'tu Tu*;h,p"o=
Male > Female (ages Male = Female (> 75 years old) Note above

b.'Who's at risk

{rr** ,f

i. MalelFemale ii.
Age

40-75)

gocr$,q"*$rUr

iii. Risk Factors -

Myocardial Infarction Hypertensive Heart Disease Negative Inotropic drugs Also note disorders listed under etiology (above)

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3. Differential Diagnosis -

Anv Voiume Overload state, such ' * Neplrotic SYndrome * Cirrirosis

as:

1"

ft-;i'lr'nr'ifa Z. t DPh"l

4.

LaboratoryIX-RaY'

E-ipt
CXR EKG ABG

Echocardiogram (BNP) ii*l

:{'

3 r+yp<rl)PCe'ni6\
tast

t{orr'-'

Prd&JL'{c

[nesiritide] natiiretic peptide sensitivitlt; > 98% spectftcitvl -Jioo t>'gi%

cBc
Serum Chemistries Drue Levels
Sear-ch for an underlYing cause

5. Treatment Plan a'

if established Searchfor Reversible Etiologl & Treat

tYI e

b' Lifes

Mo

dif

cati on.

- Sodium Restiction
- Cigarettes - Weight Loss - PhYsical ActivitY

Edema c. Medications.for Acute Pulmonarv

- Oxygen - Diuretics
LooP - Digitaiis @igoxin ILANOXN])
-

L"giot"ntin donverting
* Nitates

Enzyme (ACE) Inhibitors

- Vasodilators
- MorPhine

t gggit DYsfu,nction
o
cornerstone of treatment ,Fffi-THF t'- l--Reduce afterload

Reduceneurohormonalabnormailities Slow the Progression

- lf AcE lnhibitors contraindicated or not tolerated, options are: C"t"ptoiBlockers (- AA$'j )

'

Angioteiii"
AmlodiPine

Hyiralazine plus lsosorbide dinitrate

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frtV.c\ {i. E5"^st

'

ot^rr: g'#"h1ar"tnncs *-An'Y1n'''1rts

B. Beta-Blockers Should be used in NYHA Classification ll - lll lnitiate at a loew dose lncrease dose not more often ihan every two weeks Monitor for signs of decompensation: Fluid accu mulation (congestion) Bradycardia Heart Block Hypotension

'T

C\as:

jI.

jtr "Itr

C. Digoxin Reduces hospitalization rate, but neutral effect on mortality lncreases ejeciion fraciion - 4 - 5 % Reduce neurohormonal abnormalities Effect on baroreceptor abnormalities * Atrial fibrillation (rate unconirolled) and EF < 30 %

(LANOXIN)

Syshllc itF ;
k\ri-r"t
Fbnr\hci\L)"r

D. Diuretics

For symptomatic volume overload

May redrrcp the cardiac output (may not be the effect you want) ay cause folate rsveverrrv,rq,,rJ Spiranolactone has been shown to reduce
.._

h.ra.:,K*\{-rn n,1 .- G rrv.\ru'r".;rsxi?*.

Oepletion *ro**,.*^^kJ t' r mortality nru*_aipn.rls

{" f,rf^f6- "r-

/'1 gtt- Jd )

A. Treatment is generally directed toward the underlying problem

Hypedension Valvular Heart Disease

6. Follow Up

a.

Patient Education Educate @ Underlying problerns Educate on reducing cardiovascular risk factors Dietary management (sodium restriction) Weight loss lnformation regarding drug side effects

b. Fuhrre Appointments
Weekly (or more frequently) as needed, until stable

c.

Emergency Visits Signs/Slenptons of decompensation Respiratory/Cardiovascular dysfunction

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